Wednesday, August 24, 2011

Obesity, Salt, Exercise and Blood Pressure in Children : Dietary Salt Intake & BP in Childhood

Stella Stabouli†1,2, Sofia Papakatsika2, and Vasilios Kotsis2 Dietary Salt Intake & BP in Childhood The International Study of Salt and Blood Pressure (INTERSALT) has provided strong evidence for the association between dietary sodium and elevated BP in adults, especially in Western societies. Yanomamo Indians in the Amazon, who have a low-salt intake, present with a low average BP, no HTN and no positive slope of BP with age. There is also substantial evidence that a reduction in salt intake lowers BP and can prevent HTN and adverse cardiovascular outcomes. Most studies in children show that the average daily salt intake exceeds nutritional needs. As dietary habits create nutritional patterns for the young population, contamination of foods rich in salt increases over time in modern societies, emerging the need for prevention strategies that will reduce sodium exposure in the young through dietary modification. The effect of salt intake may begin early in life. A randomized trial, conducted among 476 Dutch newborn infants, studied the effect of low or normal sodium diets on BP. Infants fed with a low sodium diet had 2.1 mmHg lower SBP than those under a normal sodium diet at the age of 6 months. A subset of these populations was re-examined 15 years later. SBP and DBP at adolescence were 3.6 and 2.2 mmHg lower, respectively, in subjects assigned to the low sodium compared with the control group. Most observational epidemiological studies on salt and BP in children showed a significant positive association between dietary sodium and BP. However, in a study among Spanish school children, urinary excretion of sodium did not correlate with BP, whereas bodyweight correlated directly with BP and salt intake. The investigators assumed that the BP-raising effect of increased dietary sodium might not be seen until a certain age. Moreover, Howe et al. reported that dietary short-term sodium interventions, consisting of a 4-week high-salt diet following 4 weeks low-salt administration, had no significant alterations on BP levels in adolescents. A more reliable estimation of the sodium effects on BP could possibly be seen after a longer time period of sodium restriction. Sinaiko et al. enrolled 13-year-old adolescents in a study of 3-year period sodium interventions. Adolescent girls receiving a low-salt diet, presented a decrease in urinary sodium excretion and a slight decrease in BP levels. A recent meta-analysis of 13 controlled trials on salt reduction in children demonstrated that even a modest reduction in sodium intake causes immediate decreases in BP, and suggested that it may well lessen the subsequent rise in BP with age. The changes in salt intake were assessed by 24-h urinary sodium in four trials, overnight urinary sodium in three trials, spot urinary sodium/creatinine ratio in two trials, spot urinary sodium in two trials, food diary in one trial and random 24-h urinary sodium in one trial. Among the 13 trials, ten were in children and adolescents and three were in infants. The median reduction in salt intake was 42% (interquartile range: 7–58%) in children and adolescents and 54% (interquartile range: 51–79%) in infants. Individual variations in response to high or low sodium intake impact on BP define salt sensitivity or resistance. Children genetically predisposed to develop HTN, such as African–Americans, as well as those with a family history of HTN, more likely exhibit increased salt sensitivity. Simonetti et al. described the highest prevalence of salt sensitivity in children with intrauterine fetal growth retardation, born small for gestational age. In this study, salt sensitivity was defined if mean 24-h BP increased by 3 mmHg on a high-salt diet and was present in 37% of the low birthweight children. Kidney volume and length measured by ultrasound were reduced in low birthweight children and correlated with increased salt sensitivity, suggesting that a deficit of the normal nephron function in children with low birthweight, may lead to increased salt sensitivity and HTN. A similar relation of birthweight to salt sensitivity has been reported in adults. Several investigators examined the impact of salt sensitivity on the circadian variation of BP. Nondipping status, which is considered an early predictor of cardiovascular and renal complications, has been associated with increased salt sensitivity in hypertensive adults. It is assumed that in individuals with high-salt sensitivity, sodium retention and diminished excretory capability leads to elevation in nighttime BP values. This nocturnal HTN compensates for diminished natriuresis during the daytime and enhances pressure natriuresis during the night. Studies with regard to nondipping pattern and salt sensitivity in children and adolescents are controversial. Salt sensitivity has been associated with nondipping status in salt sensitive normotensive black adolescents. However, in a study conducted by Simonetti et al. normotensive children and young adults maintained normal nocturnal BP dipping independently of salt intake and sensitivity.In the same study, a steeper downward slope of BP from daytime to nighttime was observed in salt-sensitive as compared with salt-resistant children and in both groups of adults. The findings of this study may show that a time interval is needed for blunted dipping to develop, as in children the excretory sodium capacity seemed less affected than in young adults with longer exposure to salt. Salt sensitivity has been reported to involve endogenous ouabain, a modulator of the sodium pump in humans. In prehypertensive and hypertensive individuals, circulating levels of endogenous ouabain are not properly regulated in relation to sodium balance. The main mechanism of endogenous ouabain action, which has been described in animal models, may be an elevation in total peripheral resistance.In normotensive rats, acute elevations in salt intake lead to impairment of the muscular arteriolar response to vasodilator agonists in 3 days.The same effect was reported in normotensive and in reduced renal mass hypertensive rats receiving a high-salt diet for 4 weeks. In normotensive rats, impairment of the vascular function was proportionate to the remodeling of the microvessel wall, so that the sodium sensitivity remained unchanged. In reduced renal mass hypertensive rats the effects on the structure of microvessels was greater and resulted in increased sodium sensitivity and HTN. Despite the major role that sodium plays in the development of HTN in children and adolescents, salt sensitivity should be characterized as one component of the whole spectrum of cardiovascular risk factors. Sensitivity to sodium or high-salt intake alone may not directly cause a hypertensive profile, but could be interrelated to other factors, such as family history of HTN, race and obesity, which altogether contribute to the development of HTN and an adverse cardiovascular profile

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